Over the past century twin studies have been used to explore how nature and nurture influence individual differences in human characteristics (such as personality, intelligence or height). Identical twins share the same genes, while non-identical twins share about half of the same genes; but both types of twins grow up in the same family environment. This means that researchers can compare similarities between identical twins, and similarities between non-identical twins, to get an idea about how much differences between people in characteristics such as height are caused by nature (genes), and nurture (the environment).

The Health Behaviour Research Centre set up the Gemini twin cohort in 2007. Gemini is a landmark study of early life growth and behaviour which has been following 2400 British families with twins born in 2007. Gemini was established to help understand how genes (nature) and the environment (nurture) influence the development of eating behaviours, food preferences and growth in early childhood. Previous studies conducted by the Gemini team have suggested that individual differences in eating behaviours during childhood are strongly influenced by genes.

Like much research into early child development, these studies have had to rely on parents’ ratings of their children’s eating behaviour. This is because large sample sizes make it difficult to measure behaviours in a laboratory and because young children are unable to report accurately on their own characteristics. Parents of Gemini twins provided information about their children’s behaviour using a widely-used questionnaire called the Child Eating Behaviour Questionnaire (CEBQ). However, a criticism of twin studies is that parents might be biased by their beliefs about their twins’ zygosity (whether they are identical or non-identical) when rating each of their eating behaviours. For example, parents of identical twins might rate them more similarly simply because they think of them as ‘two peas in a pod’, while parents of non-identical twins might exaggerate the differences between them. Because twin studies are based on the comparison of similarity between identical and non-identical twin pairs, reliable and unbiased parental ratings are crucial.

We recently published a new study that set out to test if parents are biased by their twins’ zygosity when they rate their eating behaviours. Using the Gemini sample we compared eating behaviour ratings from parents who held a false belief about their twins’ zygosity (i.e. they believed them to be non-identical, when they were in fact identical) to those from parents who held an accurate belief. The only way to conclusively know whether a twin pair is identical is to conduct a genetic test, which compares the DNA of the two siblings. However these genetic tests are not routinely carried out and parents can sometimes be misinformed about their twins’ zygosity. A more thorough account of why these misunderstandings occur has been discussed in a previous study.

We established whether the Gemini twins were identical or non-identical using a combination of DNA testing and a questionnaire that accurately measures twin similarity. We also asked parents about whether they thought their twins’ were identical or not. Using this information we were able to identify parents who held a false belief about their twins’ zygosity, and those who were right. We found that approximately one third of parents of identical twins falsely believed them to be non-identical when they were about eight months old.

In order to test if parents’ ratings of their twins’ behaviours are biased by their beliefs about their zygosity, we compared the ratings of parents with false and accurate beliefs about their twins’ zygosity, on a range of eating behaviours during infancy and toddlerhood. If parent ratings were biased then we would expect identical twins whose parents believed them to be non-identical to be rated as less similar than identical twin pairs correctly identified by their parents as identical.

Interestingly, parents’ reports of their identical twins’ eating behaviours were the same, regardless of whether they had false or accurate beliefs about their twins’ zygosity. In other words, parents rated identical twins as more similarly than non-identical twins on all eating behaviours (in both infancy and toddlerhood), regardless of whether they believed them to be identical or non-identical. This indicates that parents of twins can be relied upon to provide unbiased reports of their young children’s eating behaviour, and that findings from twin studies can be trusted.

On 20th October, we lost the Director of our Health Behaviour Research Centre. Professor Jane Wardle, one of the UK’s leading health psychologists, was an extraordinary woman. She had an apparently insatiable appetite for research and new ideas, and the breadth of her expertise was simply awesome. She nurtured us, her PhD students and staff, to develop into independent researchers and supported us when we had personal difficulties. There was always laughter coming out of her office when she was in meetings and Jane’s door was always open to us. We miss her terribly.

While much has been written and said about her achievements and how extraordinary she was by Cancer Research UK, in the Guardian, Lancet, BMJ, The Times, The Psychologist and on Radio 4, we wanted to write about the science behind just a few of her contributions to behavioural science in cancer prevention. Over the next few weeks, our blog will do just that, starting with Jane’s work on understanding the causes of obesity written by Dr Clare Llewellyn and Dr Ali Fildes.

Our understanding of the causes of obesity

Professor Jane Wardle revolutionized our understanding of the genetic basis of human body weight. She was particularly interested in advancing our understanding of the causes of obesity because obesity is an important risk factor for cancer. In fact, obesity is the most important known avoidable cause of cancer after smoking.

We have known for many years that weight has a strong genetic basis. Importantly, Jane established that weight is as heritable now as it was 30 years ago, despite the recent large increases in obesity. This observation has been difficult for researchers to explain given the changes to the food and activity environments that are widely believed to have caused the rising rates of obesity. Researchers were confronted with the question, how can obesity be caused by both genes and the environment at the same time?

In order to answer this question, Professor Wardle developed the ‘Behavioural Susceptibility Theory’. She proposed that genes could be influencing weight through their effects on appetite. The key idea was that individuals who inherit a set of genes that make them more responsive to food cues (want to eat when they see, smell or taste delicious food), and less sensitive to satiety (take longer to feel full) are more susceptible to overeat in the current food environment, and become obese.

After finding out that appetite is already highly heritable by age 10, Jane realized that she needed to go right back to the beginning of life to explore how genes are influencing appetite and weight from birth. She therefore established Gemini – the largest study of twins ever set up to study genetic and environmental influences on weight from birth. The Gemini study includes over 2400 British families with twins born in 2007, and has now been running for over 8 years. Under Jane’s leadership Gemini has become an internationally recognised study that has advanced our understanding of childhood growth. The success of the study can be measured in its numerous publications on a range of topics from appetite, to food preferences, sleep, physical activity and the home environment. Jane loved the Gemini study, and it shone through in every aspect of her work, from discussions about complex genetic analyses to the design of the annual newsletter sent to the many dedicated families who participate. In total, Gemini has trained (and continues to train) 7 PhD students, 5 postdoctoral researchers, and numerous MSc students. The Gemini team miss Jane terribly but are committed to continuing her incredible legacy.

These are exciting times for people working in genetics. The field has become trendy. ‘DNA’, ‘genes’ and ‘genetic code’ are no longer specialist terms, but used casually in everyday language. The media love ‘The gene for’ stories and attributing individual differences to biology and less to environment is becoming commonplace. I recently read an interview with a singer who explained that she could not imagine being anything else but a singer, because singing ‘was in her DNA’. If this still does not convince you: The pop band ‘Little Mix’ recently released a new song titled ‘DNA’ (http://www.youtube.com/watch?v=D3h-lLj3xv4).

Why the fascination with genes? To a degree, it appears to stem from the inherent assumption that our genes can give us insights into ourselves that would otherwise remain inaccessible. Although our DNA is 99.9% identical, this is not interesting – it is all about the tiny bit of difference, the bit which sets us apart and makes us unique.

Companies have been quick to capitalise on our curiosity of what would be possible once the Human Genome was decoded. Genetic tests for an array of traits and conditions, including those that are common and driven by lifestyle, such as obesity or heart disease, are already available over the Internet. So far, we are not sure about the effects of giving this type of information to people. It could be that people will use it to prevent the condition. Alternatively, it could be that they become fatalistic or complacent. I have written in more detail about the current debate in a previous blogpost ( http://tinyurl.com/bve6y2m). I hope to add some evidence to the debate by looking at the psychological and behavioural consequences of receiving genetic test feedback using obesity as an example for a very common, very complex condition.

Because we do not know yet how people react to knowing about their genetic susceptibility to weight gain, it would be unwise to give them this information right away. Instead, we set up an online study where people were asked to imagine their reactions to receiving a ‘higher-risk’ or an ‘average-risk’ genetic test result for weight gain. They were then asked questions on a broad range of feelings and behaviours. We included 2 sets of people, nearly 400 students, who were predominantly of healthy weight and almost as many people from the general public who were or had been overweight.

Results showed that people in both groups reported to be more motivated to make lifestyle changes after imagining getting a ‘higher’ genetic risk result than after imagining getting an ‘average’ genetic risk result. On average, negative feelings and feelings of fatalism were anticipated to be very low and did not differ between risk scenarios. Those who were already overweight or obese were more likely to think that in comparison with an ‘average’ genetic risk result, receiving a ‘higher’ genetic risk result would offer them an explanation for their weight status. Finally, people in both groups thought that they would be more likely to seek out information about what their result means in the ‘higher-risk’ than in the ‘average-risk’ scenario.

These findings are good news, because they suggest that giving people feedback for susceptibility to weight gain is unlikely to have unanticipated negative effects, and may even be motivating. Furthermore, people who are already overweight may also benefit from genetic feedback. However, these findings may not hold up once people are actually given genetic test feedback, because they only tell us about what people think they might do – and people find it generally quite difficult to imagine to be negatively affected by an event. The next step is now to give people ‘real’ genetic feedback for risk of weight gain to discover the effect of this type of information.

All animals need it, we go crazy without it, yet, we don’t understand it well – no, I am not talking about love here, but a much less considered, although just as profound, need: The need for sleep.

Sleep is currently a ‘hot topic’ in science, because it appears that it is vital for all other major systems in our brains and bodies to function well – from how we feel , how well our muscles function, how well we concentrate, to the food choices we make. Moreover, there is growing evidence that shorter sleep is linked with a large number of diseases, such as obesity, heart disease, cancer, lowered function of the immune system and mental health problems.

Although, as a nation overall, we sleep less than ever before, individuals vary substantially in the need for sleep –your partner may be chirpy after 7 hours, whereas you may need more to feel human. Interestingly, variation occurs even in the same families and among siblings; this raises the question of whether genes play a role in determining how much sleep a person needs, because families usually share a very similar environment. However, very few large studies have looked at what influences sleep early in life, when sleep is assumed to be mainly governed by the infant’s ‘body clock’. Twins are especially useful to tease the question of ‘nature’ and ‘nurture’ apart, because twins are either 100% genetically identical; or they share half of their genes, just as ‘normal’ siblings. Both, however, usually share the same environment, because they are born at the same time. Our researchers used data from the GEMINI birth cohort, which includes twins from about 2000 families, to take a closer look at the genetic and environmental influences of sleep in young children.

Perhaps surprisingly, the results showed that sleep duration and daytime nap duration were mainly influenced by the environment. Likewise, sleep disturbance was due to environmental influences, although the genetic effect was slightly bigger than for sleep duration. This was true for both girls and boys. Although it could be argued that the carer’s schedule determines infants’ sleeping time, it would be expected that they would adjust bed-and nap times according to the infants’ needs. Unfortunately there was no data available on when the infants actually went to sleep once they were put to bed, so we cannot say for sure how long they actually slept.

This study shows that, as so often, nature and nurture both act together to influence how we behave; in this instance, how much and how well we sleep. Nonetheless, the study is important, because it shows that being a ‘morning vs. evening’ type person is indeed influenced to an extent by genes and this is apparent already very early in life. However, what is more important, the study clearly shows that the home environment is a crucial factor for providing children with a good night’s sleep. So, it might be wise to practice good ‘sleep hygiene’ (and that is not only true for kids): Remove the TV from the bedroom, have a consistent bedtime routine, put your kids to bed before 9pm if they are under 10 years old, let them fall asleep without anyone present, and limit (soft) drinks containing caffeine. That will, hopefully, help your kids, and ultimately you, too, to get the well-deserved snooze.

Mentioning genetics in the context of weight is like treading into a minefield; those who are brave enough to approach the topic need to don their hard hats and be prepared to take hits by followers in the ‘eat-less-and-move-more’ camp. Accusations of laziness, lack of willpower, making excuses and just looking for an easy way out are common responses to the genetic argument of obesity.

However, to ignore genetics when talking about obesity is somewhat confusing when considering how keen people are to attribute skinniness to ‘good genes’, ‘fast metabolism’, and ‘being naturally active’. Nobody seems to notice that skinniness and fatness are two sides of the same coin.

As so often in life, the truth lies somewhere in between. While behaviour is certainly not to be ignored when searching for the root cause of the obesity epidemic, neither should the heritability of body weight. Two recent studies from our research group add evidence to the idea that the predisposition to thinness, as well as to overweight, is transmitted across generations. Researchers used data from the Health Survey for England, which included a large sample of families with children aged 2-15 years to see whether thin children were more likely to have thin parents. Of the thousands of families included in the first study, it was shown that thin children were almost twice as likely to have 2 thin parents. Furthermore, as parents’ weight decreased, children likewise got progressively lighter.

But, what about the reverse side of the coin – parental weight of children who were overweight? Here, exactly the same pattern was found, but it was even more apparent. Children, who had 2 obese or severely obese parents, were approximately 12 times more likely to be overweight and again the likelihood of obesity gradually decreased with decreased parental body weight. In both studies, findings were unrelated to other factors such as age, sex, social status or ethnicity. Interestingly, the mothers’ weight seemed to be more predictive of a child’s than the father’s, but only among those children that were overweight. For thin children, mothers’ and fathers’ genes appeared to contribute equally to being thin.

Two things are important here. Firstly, weight is governed in part by genetic factors; but, and this is the second important conclusion to take away, there are environmental factors involved that influence a child’s weight – otherwise all children would have had parents that fully resembled their weight status. Influences seem to come especially from the mother’s side, which may be, because the foetus receives nutrients from the maternal diet in the womb and after birth when the infant is breast-fed. In addition, maternal environmental influences may be stronger because the mother is usually in charge of food preparation.

Unfortunately, dietary records of participants were not available, so it was not possible to investigate how diets between underweight and overweight children and their parents differed.

Genes do not always act in the same way; their activity is influenced by the environment. This flexibility allowed our species to adapt well to changing environmental conditions, which made it possible to survive and evolve. Variation is the key. And this is why it is easier for some than for others to (not) have their cake and eat it, too.